Orthodontic treatment and periodontal disease can have an inter-conditional relationship, particularly when the accumulation of bacterial plaque, favoured by orthodontic appliances and poor oral hygiene can cause periodontal inflammation. The objective of the study is to highlight the influence of the risk factors’ polymorphism on the therapeutic response in periodontal disease. 64 patients with mixed or definitive dentition and poor oral hygiene were included in the study, of whom 22 patients followed treatment with fixed orthodontic dispensers, 22 patients were treated with mobile orthodontic braces and 20 were non-attendants. From all patients gingival crevicular fluid was collected and assessed, before and after applying a chlorhexidine-based gel antiseptic agent.
Periodontal disease is a chronic pathology, resulting from the action of microbial communities that become dysbiotic, accompanied by immune response impairment in periodontal tissues, leading to an inflammatory process that promotes progressive tissue destruction. Abnormal activation of nucleotide-binding oligomerization domain (NOD-), leucine-rich repeat (LRR-), and pyrin domain (PYD)-containing protein 3 (NLRP3) promotes chronic inflammation. Research shows that leptin and oxidative stress (OS) are involved in the activation of the inflammatory pathways, including the activation of the NLRP3 inflammasome. In this context, the main objective of our study was to determine the levels of the NLRP3, leptin, and total antioxidant capacity (TAC) in the saliva of patients with periodontal disease. The present cross-sectional study included 44 patients with periodontitis, while the control group was represented by 19 clinically and biologically healthy adults. Saliva samples were collected from all participants in the study, and salivary levels of NLRP3, leptin, and TAC were determined using the Enzyme-linked immunosorbent assay (ELISA) and commercial kits. The results show that NLRP3 had statistically significantly increased levels in the study group versus the control group (p< 0.00001). Although TAC was also increased in the patients compared to the healthy subjects (p=0.491), no statistically significant differences were found. On the other hand, leptin levels were significantly lower in periodontitis patients compared to the control group (p< 0.00001). The results obtained in the present study are promising, but further studies are needed to obtain a more comprehensive understanding of the complex molecular mechanisms underlying periodontal disease.
